Cloning and tissue distribution of the human 1 lβ-hydroxysteroid dehydrogenase type 2 enzyme

Association between a variant in the 11β-hydroxysteroid dehydrogenase type 2 gene and primary hypertension

“…1 However, the enzyme 11␤-hydroxysteroid dehydrogenase type 2 (11BHSD2) protects the mineralocorticoid receptor from the mineralocorticoid actions of cortisol by converting cortisol to cortisone. [2][3][4] Cortisone has a low affinity for the mineralocorticoid receptor 5,6 and aldosterone is therefore the major mineralocorticoid in vivo. The 11BHSD2 gene is located on chromosome 16q22 7 and is expressed at high levels in the kidney, colon and placenta.…”

“…The 11BHSD2 gene is located on chromosome 16q22 7 and is expressed at high levels in the kidney, colon and placenta. 4,8,9 The syndrome of Apparent Mineralocorticoid Excess (AME) is a rare monogenic form of hypertension with autosomal recessive inheritance and is caused by homozygous or compound heterozygous Correspondence: Olle Melander, Department of Endocrinology, Malmö University Hospital MAS, S-205 02 Malmo, Sweden. Fax: 00 46 40 337042, E-mail: Olle.MelanderȰendo.mas.lu.se morphism was identified in exon 3; G534A (Glu178Glu).…”

Effect of hyperlipidemia on 11β-hydroxysteroid-dehydrogenase, glucocorticoid receptor, and leptin expression in insulin-sensitive tissues of cats

“…11β-HSD2 utilizes NAD to inactivate cortisol to cortisone. It serves to protect the mineralocorticoid receptor (MR) from cortisol excess and is expressed in MR-rich tissues, such as kidney, colon and salivary glands [8,9]. A pathogenetic role of 11β-HSD1 in insulin resistance is supported by several animal models.…”

Expression of 11β-hydroxysteroid-dehydrogenase 2 in Sertoli cells of boar testes

“…More recently, research was focussed on the 11ß-hydroxysteroid-dehydrogenase enzymes (11ß-HSD), which play a role in the pre-receptor regulation of glucocorticoid hormone action (for review see Draper and Stewart, 2005). Two isoforms were characterized: 11ß-HSD2 is a unidirectional high affinity enzyme which oxidizes active cortisol to inactive cortisone in the presence of NAD + as a cofactor (Albiston et al, 1994;Brown et al, 1993). Initially, its function in aldosterone sensitive tissues was investigated, e.g.…”